The overall objective of this research is to investigate the neural structures and mechanisms regulating hypothalamo-pituitary functions in the rat. Most effort will be directed at the control of growth hormone (GH) and the role of somatostatin (SRIF) in this control and in regulating thyrotropin (TSH) secretion under certain conditions. Other projects deal with the control of prolactin (Prl) and pituitary-adrenal function. Our previous studies indicate that hypothalamic lesions can differentially disrupt the inhibitory control of GH and TSH secretion. One of the GH-SRIF projects will test the hypothesis, by placement of discrete neural lesions, that anatomically-separate pools of neurons are responsible for inhibiting GH secretion under nonstress conditions, suppressing GH secretion in response to stress and inhibiting TSH secretion under non-stress and stress conditions. Another project will determine whether the hypothalamic SRIF system continues to control GH and TSH secretion after lesion-induced depletion of median eminence SRIF; passive immunization, electrical stimulation, perifusion of hypothalamic and pituitary tissues in vitro and immunocytochemistry will be used as approaches. Finally, several experiments will examine further the relationship between plasma GH levels and increased linear growth in rats with hypothalamic lesions by studying effects of gonadectomy and changes in food intake. One Prl project will attempt to identify further, through placement of lesions, the forebrain structures essential for stress-induced stimulation of Prl secretion. Another study will determine the basis for the deficits in the control of Prl secretion produced by surgical interruption of anterolateral connections of the medial basal hypothalamus (MBH) using in vitro perifusion of MBH and pituitary tissues. The pituitary-adrenal projects will reassess the effects of severing anterolateral connections of the MBH on responses to certain stressful stimuli. If the results support prior findings and indicate that responses to some stressors persist in the absence of such conections, the roles of the adrenal medulla, superior cervical ganglia, renin-angiotensin system and systemic circulation will be studied. If anterolateral connections are essential, the source or such connections will be sought with discrete brain lesions.